Viroids are small single-stranded, circular RNAs that are infectious pathogens.[1][2] Unlike viruses, they have no protein coating. All known viroids are inhabitants of angiosperms (flowering plants),[3] and most cause diseases, whose respective economic importance to humans varies widely.[4] A recent metatranscriptomics study suggests that the host diversity of viroids and other viroid-like elements is broader than previously thought and that it would not be limited to plants, encompassing even the prokaryotes.[5]
The first recognized viroid, the pathogenic agent of the potato spindle tuber disease, was discovered, initially molecularly characterized, and named by Theodor Otto Diener, plant pathologist at the U.S Department of Agriculture's Research Center in Beltsville, Maryland, in 1971.[7][8] This viroid is now called potato spindle tuber viroid, abbreviated PSTVd. The Citrus exocortis viroid (CEVd) was discovered soon thereafter, and together understanding of PSTVd and CEVd shaped the concept of the viroid.[9]
Although viroids are composed of nucleic acid, they do not code for any protein.[10][11] The viroid's replication mechanism uses RNA polymerase II, a host cell enzyme normally associated with synthesis of messenger RNA from DNA, which instead catalyzes "rolling circle" synthesis of new RNA using the viroid's RNA as a template. Viroids are often ribozymes, having catalytic properties that allow self-cleavage and ligation of unit-size genomes from larger replication intermediates.[12]
Diener initially hypothesized in 1989 that viroids may represent "living relics" from the widely assumed, ancient, and non-cellular RNA world, and others have followed this conjecture.[13][14] Following the discovery of retrozymes, it has been proposed that viroids and other viroid-like elements may derive from this newly found class of retrotransposon.[15][16][17]
The human pathogen hepatitis D virus is a subviral agent similar in structure to a viroid, as it is a hybrid particle enclosed by surface proteins from the hepatitis B virus.[18]
^Di Serio F, Owens RA, Li SF, Matoušek J, Pallás V, Randles JW, Sano T, Verhoeven JT, Vidalakis G, Flores R (November 2020). Zerbini FM, Sabanadzovic S (eds.). "Viroids". Archived from the original on December 2, 2020. Retrieved February 3, 2021.
^Flores R, Hernández C, Martínez de Alba AE, Daròs JA, Di Serio F (2005). "Viroids and viroid-host interactions". Annual Review of Phytopathology. 43: 117–39. doi:10.1146/annurev.phyto.43.040204.140243. PMID16078879.